Enterococci are intrinsically resistant to various antimicrobial classes and able to acquire resistance to clinically relevant drugs via chromosomal mutations and horizontal gene transfer. Consequently, therapeutic options for treatment of enterococcal infections are limited. Zoonotic transfer of antimicrobial resistance in enterococci has been studied for many years. The first studies hypothesizing possible animal-to-human transmission of resistant strains and mobile genetic elements are dated 1993. Since then, a considerable amount of papers has been published on this subject, providing the groundwork for important decisions limiting antimicrobial use in animal husbandry. In this chapter, the relative contribution by animal enterococci to antimicrobial resistance in infections in humans was reviewed taking into consideration the potential impact associated with different enterococcal species, animal hosts, epidemiological routes, and mechanisms of transfer. The authors conclude that potential zoonotic risks mainly concern horizontal transfer of resistance genes and clonal transmission of multidrug-resistant Enterococcus faecalis lineages such as ST16 from a variety of animal species. The risk of clonal transmission appears to be negligible for Enterococcus faecium, which is markedly more host-specific than E. faecalis, and mainly limited to companion animals, which are a potential reservoir of ampicillin-resistant, hospital-associated lineages such as ST78 and ST192. Of note, such conclusions are largely based on studies from developed countries that never used or banned the use of antimicrobial growth promoters in livestock for nearly two decades (at the time of writing this review), which has significantly reduced the occurrence of resistance to clinically relevant antimicrobials in enterococci in animals. As for horizontal transfer of mobile genetic elements, although it has been demonstrated experimentally that antimicrobial-resistant enterococci of animal origin can transiently colonize the human digestive tract and transfer their resistance genes to the indigenous microbiota, the magnitude and clinical implications of this phenomenon, which currently appear to be limited, have not been fully elucidated. Further research is warranted to explore the ecology and epidemiology of enterococcal mobile genetic elements carrying resistance genes of clinical relevance, especially aminoglycoside and linezolid resistance in E. faecalis.